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粒细胞巨噬细胞集落刺激因子和巨噬细胞集落刺激因子对人单核细胞中肿瘤坏死因子和白细胞介素-1产生的不同作用。

Differential effects of granulocyte-macrophage colony-stimulating factor and macrophage colony-stimulating factor on tumor necrosis factor and interleukin-1 production in human monocytes.

作者信息

Essner R, Rhoades K, McBride W H, Morton D L, Economou J S

机构信息

Division of Surgical Oncology, John Wayne Cancer Clinic, Armand Hammer Laboratories, Los Angeles, California.

出版信息

J Clin Lab Immunol. 1990 Aug;32(4):161-6.

PMID:1966932
Abstract

Human peripheral blood monocytes (PBM) cultured in the presence of 100-5,000 u/ml granulocyte-macrophage colony-stimulating factor (GM-CSF) for 24 hr secreted small quantities of tumor necrosis factor (TNF), but not interleukin-1 (IL-1). The activation of PBM to produce TNF was weak and could be blocked by polyclonal anti-GM-CSF anti-serum. Neither LPS nor IL-2 were synergistic with GM-CSF in the production of TNF or IL-1. IFN gamma alone did not induce either cytokine, but in the presence of GM-CSF it caused a synergistic (100-fold) increase in TNF but not IL-1 production. Macrophage colony-stimulating factor (M-CSF) alone or in combination with LPS, IFN gamma or IL-2 did not stimulate PBM to produce TNF or IL-1 in 24 hr culture.

摘要

在100 - 5000单位/毫升粒细胞-巨噬细胞集落刺激因子(GM - CSF)存在的情况下培养24小时的人外周血单核细胞(PBM)分泌少量肿瘤坏死因子(TNF),但不分泌白细胞介素-1(IL - 1)。PBM产生TNF的激活作用较弱,且可被多克隆抗GM - CSF抗血清阻断。在TNF或IL - 1的产生过程中,脂多糖(LPS)和IL - 2均与GM - CSF无协同作用。单独的干扰素γ(IFNγ)不诱导任何一种细胞因子产生,但在GM - CSF存在的情况下,它会使TNF的产生协同增加(100倍),但不会使IL - 1的产生增加。在24小时培养中,单独的巨噬细胞集落刺激因子(M - CSF)或与LPS、IFNγ或IL - 2联合使用均不会刺激PBM产生TNF或IL - 1。

相似文献

1
Differential effects of granulocyte-macrophage colony-stimulating factor and macrophage colony-stimulating factor on tumor necrosis factor and interleukin-1 production in human monocytes.粒细胞巨噬细胞集落刺激因子和巨噬细胞集落刺激因子对人单核细胞中肿瘤坏死因子和白细胞介素-1产生的不同作用。
J Clin Lab Immunol. 1990 Aug;32(4):161-6.
2
Synergistic activation of human monocytes by granulocyte-macrophage colony-stimulating factor and IFN-gamma. Increased TNF-alpha but not IL-1 activity.粒细胞巨噬细胞集落刺激因子和干扰素-γ对人单核细胞的协同激活作用。肿瘤坏死因子-α活性增加,但白细胞介素-1活性未增加。
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Granulocyte-macrophage colony-stimulating factor, but not macrophage colony-stimulating factor, suppresses basal and lipopolysaccharide-stimulated complement factor production in human monocytes.粒细胞-巨噬细胞集落刺激因子而非巨噬细胞集落刺激因子,可抑制人单核细胞中基础的及脂多糖刺激的补体因子生成。
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引用本文的文献

1
Granulocyte-macrophage colony-stimulating factor amplification of interleukin-1beta and tumor necrosis factor alpha production in THP-1 human monocytic cells stimulated with lipopolysaccharide of oral microorganisms.粒细胞-巨噬细胞集落刺激因子增强经口腔微生物脂多糖刺激的THP-1人单核细胞中白细胞介素-1β和肿瘤坏死因子α的产生。
Clin Diagn Lab Immunol. 1998 May;5(3):341-7. doi: 10.1128/CDLI.5.3.341-347.1998.
2
Enhanced killing capacity of human Kupffer cells after activation with human granulocyte/macrophage-colony-stimulating factor and interferon gamma.用人粒细胞/巨噬细胞集落刺激因子和干扰素γ激活后,人库普弗细胞的杀伤能力增强。
Cancer Immunol Immunother. 1994 Sep;39(3):179-84. doi: 10.1007/BF01533384.